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An unusual cause of a non-ST segment elevation myocardial infarction
  1. Rebecca D Levit1,
  2. Marek Polomsky2,
  3. J David Vega2,
  4. David R Martin3,
  5. Gautam Kumar1,4
  1. 1Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA
  2. 2Division of Cardiothoracic Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, Georgia, USA
  3. 3Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia, USA
  4. 4Division of Cardiology, Atlanta Veterans Affairs Medical Center, Decatur, Georgia, USA
  1. Correspondence to Dr Gautam Kumar, Cardiology Division (111C/D), Atlanta Veterans Affairs Medical Center, 1670 Clairmont Road, Decatur, GA 30033, USA; gautam.kumar{at}emory.edu

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Clinical introduction

A 66-year-old man presented with dull, left-sided chest pain for 1 week occurring mainly at rest. The symptoms had been present for 1 month but had increased in frequency over the preceding 3 days. He became acutely short of breath with substernal chest pain while climbing a flight of stairs the day of admission. The pain was pressure-like, did not radiate and was associated with presyncope, but not syncope, diaphoresis, nausea nor vomiting. He had no past medical history of cardiac disease but did have risk factors for coronary artery disease (CAD) including hypertension, history of smoking and the metabolic syndrome. His past medical history was also significant for non-Hodgkin's stage IV marginal zone B cell lymphoma treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) 4 years earlier. Vital signs and physical exam were normal without murmurs, rubs or gallops. The lung fields were clear, there was no jugular venous distention nor lower extremity oedema. A 12-lead ECG showed normal sinus rhythm without ST segment elevations and his serum troponin I was elevated to 1.69 ng/mL. He was treated medically for a non-ST segment elevation myocardial infarction and underwent non-emergent coronary angiography for recurrent chest pain. Figure 1 shows injection of right coronary artery (RCA) in left anterior oblique orientation (LAO) at the time of coronary angiography (figure 1).

Figure 1

Still frame of injection of right coronary artery in left anterior oblique orientation at the time of coronary angiography.

Question

Cardiac angiographic image is most consistent with the following:

  1. Pulmonary arterial-venous malformation with fistula to the RCA.

  2. Significant stenosis of the mid portion of the RCA.

  3. Tumour blush due to vascular tumour with blood supply derived from the RCA.

  4. Fistula between the RCA and right atrium (RA).

From the question on page 1619

Answer: C

Angiogram of the RCA showed tumour blush in the RA (figure 2A), not the pulmonary artery nor lung, as expected in a pulmonary artery fistula. RCA-RA fistula would opacify the entire atrium instead of a discrete area. There is no RCA stenosis and the left coronary artery had non-obstructive disease. Cardiac MRI and transesophageal echo confirmed a soft tissue mass within the RA (figure 2B,C). The mass was surgically resected (figure 2D) and showed high-grade angiosarcoma (figure 2E). The patient underwent chemotherapy, surviving 8 months.

Figure 2

Multimodality imaging, surgical view and histopathological appearance of an intracardiac angiosarcoma. Left anterior oblique view of right coronary artery at time of cardiac catheterisation revealed tumour blush (arrow) in vicinity of right atrium (A). Tumour was localised to the floor of the right atrium and appendage by T2-weighted, precontrast cardiac MRI (B, arrow) and by contrast-enhanced transesophageal echocardiography (C, arrow). Following median sternotomy and cannulation, a 3.0×2.5×1.5 cm angiosarcoma was seen arising from the right atrial appendage (D) and resected with bovine pericardium atrial reconstruction. H&E stain of the surgical specimen (E) showed high-grade angiosarcoma with spindle cell morphology, focal vasoformative architecture and mitotically active nuclei intermixed with background cardiomyocytes (20×).

References

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Footnotes

  • Contributors All authors had a highly significant contribution to this work. RDL drafted the article and collected images. MP, JDV and DRM collected additional surgical and pathological images and contributed significantly to manuscript revisions. GK conceptualised the format, contributed significantly to revisions and obtained clinical images.

  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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